Auswahl der wissenschaftlichen Literatur zum Thema „Maladies d'Alzheimer“
Geben Sie eine Quelle nach APA, MLA, Chicago, Harvard und anderen Zitierweisen an
Inhaltsverzeichnis
Machen Sie sich mit den Listen der aktuellen Artikel, Bücher, Dissertationen, Berichten und anderer wissenschaftlichen Quellen zum Thema "Maladies d'Alzheimer" bekannt.
Neben jedem Werk im Literaturverzeichnis ist die Option "Zur Bibliographie hinzufügen" verfügbar. Nutzen Sie sie, wird Ihre bibliographische Angabe des gewählten Werkes nach der nötigen Zitierweise (APA, MLA, Harvard, Chicago, Vancouver usw.) automatisch gestaltet.
Sie können auch den vollen Text der wissenschaftlichen Publikation im PDF-Format herunterladen und eine Online-Annotation der Arbeit lesen, wenn die relevanten Parameter in den Metadaten verfügbar sind.
Zeitschriftenartikel zum Thema "Maladies d'Alzheimer"
Dreyfus, JC. „Maladies neurodégénératives du Pacifique Ouest : relations avec la maladie d'Alzheimer“. médecine/sciences 3, Nr. 7 (1987): 426. http://dx.doi.org/10.4267/10608/3711.
Der volle Inhalt der QuelleHournau-Blanc, Julie. „Maladie d'Alzheimer et maladies apparentées approches de la fin de vie“. Jusqu’à la mort accompagner la vie N° 117, Nr. 2 (2014): 91. http://dx.doi.org/10.3917/jalmalv.117.0091.
Der volle Inhalt der QuelleHarrison, Christine. „Personhood, Dementia and the Integrity of a Life“. Canadian Journal on Aging / La Revue canadienne du vieillissement 12, Nr. 4 (1993): 428–40. http://dx.doi.org/10.1017/s0714980800011983.
Der volle Inhalt der QuelleKenigsberg, Paul-Ariel, Katalin Ersek, László Gulácsi, Kristian Karpati, Alan Jacques, Anders Gustavsson, Linus Jönsson, David Mcdaid, Hannu Valtonen und Anders Wimo. „Impact socio-économique de la maladie d'Alzheimer et des maladies apparentées en Europe“. Gérontologie et société 32 / n° 128-129, Nr. 1 (2009): 297. http://dx.doi.org/10.3917/gs.128.0297.
Der volle Inhalt der QuelleImbert, Geneviève. „Enseignement et formation dans le contexte des maladies d'alzheimer et apparentées“. Gérontologie et société 36 / n° 147, Nr. 4 (2013): 205. http://dx.doi.org/10.3917/gs.147.0205.
Der volle Inhalt der QuelleKenigsberg, Paul-Ariel, Laëtitia Ngatcha-Ribert, Marion Villez, Fabrice Gzil, Alain Bérard und Michèle Frémontier. „Le répit : des réponses pour les personnes atteintes de la maladie d'alzheimer ou de maladies apparentées, et leurs aidants ? évolutions de 2000 à 2011“. Recherches familiales 10, Nr. 1 (2013): 57. http://dx.doi.org/10.3917/rf.010.0057.
Der volle Inhalt der QuelleCouret, A., V. Gardette, A. Renoux und M. Lapeyre-Mestre. „CO3.3 - Impact des modifications du remboursement des médicaments spécifiques de la maladie d'Alzheimer et maladies apparentées en France : analyse de la cohorte FRA-DEM“. Journal of Epidemiology and Population Health 72 (Mai 2024): 202409. http://dx.doi.org/10.1016/j.jeph.2024.202409.
Der volle Inhalt der QuelleGagnon, Michèle, und Lisa Sweet. „W.D. Molloy and P.J. Caldwell. Alzheimer's Disease. Toronto, ON: Key Porter, 1998.“ Canadian Journal on Aging / La Revue canadienne du vieillissement 19, Nr. 2 (2000): 282–84. http://dx.doi.org/10.1017/s0714980800014069.
Der volle Inhalt der QuelleLasserre, Alain. „Aide et aidant, malade et maladie d'Alzheimer“. Empan 94, Nr. 2 (2014): 71. http://dx.doi.org/10.3917/empa.094.0071.
Der volle Inhalt der QuelleDelaloye, Julia, und Elsa Montavon. „Maladie d'Alzheimer : notre mode de vie comme facteur protecteur“. Cortica 2, Nr. 2 (19.09.2023): 24. http://dx.doi.org/10.26034/cortica.2023.4191.
Der volle Inhalt der QuelleDissertationen zum Thema "Maladies d'Alzheimer"
Iskandar, Samy. „Développement de formes vectorisables innovantes dans le cadre de maladies liées à l'âge“. Thesis, Aix-Marseille, 2019. http://theses.univ-amu.fr.lama.univ-amu.fr/191211_ISKANDAR_942qv952dpkqb571ugya506omy_TH.pdf.
Der volle Inhalt der QuelleAlzheimer's disease is a degenerative brain disease where abnormal chemicals accumulate causing progressive deterioration of memory and intellectual ability. It is a neurodegenerative disease that causes lesions in the brain. Irreversible lesions lead to a decline in cognitive functions, which serve to process information, and behavioral as the disease progresses. Loss of immediate memory, and then older memories, changes in judgment and reasoning, changes in mood and behavior are the main manifestations.Contrary to popular belief, Alzheimer's disease is not related to the normal aging of the brain. Today, the cost of the disease in Europe is estimated at 160 million euros/year, despite that, there is no effective symptomatic treatment.New non-drug approaches should be explored to slow the progression of the disease. Research in the field of the "Drug Delivery System" reveals increasingly promising systems. Addressing molecules of therapeutic interest to a target tissue is a major challenge in Drug Delivery. New targeting technologies have emerged. The search for vectors having a sufficiently long life in the body to reach the target area has already been put in place. This work is a modest step in the exploration of nanovectorized herbal medicine for the treatment of Alzheimer's disease
Gardette, Virginie. „Étude de l'utilisation des médicaments dans la maladie d'Alzheimer et maladies apparentées“. Toulouse 3, 2013. http://www.theses.fr/2013TOU30277.
Der volle Inhalt der QuelleThe leading cause of dementia is Alzheimer's Disease (AD). To date, the drugs marketed in AD (cholinesterase inhibitors and memantine, also called antidementia drugs) are symptomatic and of limited efficacy. In particular, the optimal treatment duration is still under debate. In addition, neuroleptics (antipsychotics) are commonly used in behavioural and psychological symptoms of dementia (BPSD). However, their use remains mostly off label and an increased mortality risk has been suggested with these agents. This led to 2 warnings in march 2004 and December 2008 issued by the French drug agency (AFSSaPS). Data about longitudinal drug use's patterns among clinically confirmed AD patients in a real-life setting remain scarce. This thesis dealt with pharmacoepidemiologic studies of antidementia drugs and antipsychotics is subjects with Alzheimer's Disease or associated disorders. The first part of this thesis aimed to (i) estimate the incidence of antidementia drugs' discontinuation and switch, and (ii) to identify predictive factors of these 2 outcomes. We conducted 2 researches in 2 cohorts. The first analysis was conducted among 611 French AD patients followed for 2 years. The second analysis was performed among a European cohort of 1375 subjects with AD followed for 2 years. We restricted this analysis to the antidementia drugs new users (n=557). The second part of this thesis aimed to study antipsychotic drug use in AD and associated disorders. We first studied the mortality risk associated with antipsychotic use in a 4-year cohort of 686 French subjects with AD. We secondarily described trends in the use of antipsychotic drugs in France between 2003 and 2011, and assessed the impact of AFSSaPS warnings. To this aim, we conducted an interrupted time series study among subjects with and without dementia in the French main Health Insurance Scheme. Patterns of drug use and proper use of medicinal drugs in AD need to be further investigated
Grznárová, Katarína. „Les relations moléculaires entre la maladie d'Alzheimer et les maladies à prions“. Paris 7, 2013. http://www.theses.fr/2013PA077291.
Der volle Inhalt der QuelleMany human neurodegenerative diseases are now considered as caused by protein misfolding and prion-like mechanisms seem to be more the rule in these processes than an exception limited to prion diseases. The normal prion protein (PrP) appears to be critical in neurodegeneration induced by Aβ oligomers in Alzheimer's disease (AD). However, PrP- Aβ interaction is not reserved only to toxic Aβ1-42 oligomers. Also monomeric Aβ1-40, naturally produced in healthy brain as non-aggregated peptides, have been shown to interact with cellular PrP. We explored here the role of the interaction between PrP and monomeric Aβ1-40 in PrP aggregation process. To this aim, PrP and Aβ1-40 were produced as highly pure and monodisperse recombinant proteins. We show here a clear positive effect of Aβ1-40 on PrP aggregation. Moreover, we demonstrate that Aβ1-40 naturally binds to two distinct N-terminal regions of PrP and subsequently to a third binding site created after structural rearrangement of PrP globular domain, which contributes to enhance the oligomerization rate of the complex. These results bring new insight into the mechanisms of the physiologically relevant PrP-Aβ1-40 interaction as well as into key structural changes that might be involved in prion diseases
Quoniam, Nolwenn. „L'apathie dans la maladie d'Alzheimer et la démence fronto-temporale“. Paris 5, 2007. http://www.theses.fr/2007PA05H048.
Der volle Inhalt der QuelleThis thesis examined mechanisms of apathy in Alzheimer's disease (AD) and fronto-temporal dementia (FTD). Therefore we included 36 AD, 13 FTD and 29 control subjects. Results showed different profiles of apathy depending on the pathology : among the FTDs, apathy was global, involving all activity fields, whereas among the Ads, apathy was selective, involving only some activity field. Each of these apathy profiles was related to different psycho-affective and behavioural disturbances. The FTDs showed dysexecutive syndrome related with frontal behavioural troubles. On the contrary, ADs showed less important executive and frontal perturbations related to other troubles (depression) that do no exist among the FTDs. Apathy seemed related with organic mechanisms (because evolving with the intensity of the cognitive deficiency) and/or psycho-affective mechanisms (depression, anxiety due to repeated failures)
Costes, Ghyslaine. „Les anticholinestérasiques dans la maladie d'Alzheimer“. Bordeaux 2, 1999. http://www.theses.fr/1999BOR2P057.
Der volle Inhalt der QuellePariente, Antoine. „Impact des inhibiteurs de l'acétylcholinestérase dans la maladie d'Alzheimer et les maladies apparentées“. Bordeaux 2, 2008. http://www.theses.fr/2008BOR21574.
Der volle Inhalt der QuelleMore than 850 000 persons are affected by Alzheimer's disease (AD) and other dementias in France. The clinical meaning of the efficacy of cholinesterase inhibitors (Ch1s) in these indications remains controversial. The objective of this thesis was to estimate the impact of Ch1s in population in the treatment of AD and other dementias. Firstly, we studied the use of Ch1s in the population : 20 % of demented patients could use Ch1s in France, among whom 45 % would present one-year persistence to treatment, the persistence being lower for older or paucisymptomatic patients. These factors could thus lmit the potential impact of Ch1s. Secondly, we studied the efficacy of Ch1s in the population : Ch1 use, without considering its patterns, was not associated with a decreased risk of rapid cognitive decline. Conversely in treated patients, non-persistence was associated with a two-fold increase in the risk of institutionalisation or death. Ch1s could thus have a clinically meaningful efficacy providing that their patterns of use warrant a sufficient persistence. Thirdly, we studied the safety of Ch1s in the population : the risk of severe adverse events, among all events, was higher for patients treated with Ch1s using psychotropics. The use of antipsychotics was associated with an increased risk of myocardial infarction, without any interaction with the use of Ch1. These results could help reconsidering the interest of Ch1s in the treatment of AD and other dementias. They also allowed to identify the populations in which the patterns of use of Ch1s were the most likely to compromise their therapeutic benefit and should be optimized to improve the impact of these drugs
Loiseau, Valérie. „La maladie d'Alzheimer : à la recherche d'une stratégie thérapeutique“. Bordeaux 2, 1995. http://www.theses.fr/1995BOR2P090.
Der volle Inhalt der QuelleWallon, David. „Phénotypes de la maladie d'Alzheimer génétiquement déterminée et identification de nouvelles causes“. Rouen, 2014. http://www.theses.fr/2014ROUENR01.
Der volle Inhalt der QuelleOur objective was to study the phenotypes and genetic abnormalities related to early-onset Alzheimer Disease. The proportion of mutations leading to an autosomal dominant inheritance was: 51% for PSENT, 6% for PSEN2, 11% of APP mutations and 9% of APP duplications. The limits and means (m) of the age of onset were respectively: [24-63 years] (m=43. 6); [53-69] (m=55. 9); [35-61] (m=50. 8) and [41-65] (m=51. 3). Classical AD was the main phenotype (82%) but in 18% of cases, the phenotype was atypical Among patients harboring PSEN1 mutations, we described spastic paraplegia (14. 8%), frontal variant (10. 8%), ataxia (5. 4%) or early seizures (19. 6%). Seizures were more frequent in APP duplications (31. 2%). The cerebrospinal fluid (CSF) biomarkers were indicative of AD in 90% of these patients. In case of discrepancy between clinical and biomarker conclusions, 76. 9% of clinicians changed their final diagnosis according to the CSF biomarkers. However, a limit of these biomarkers was illustrated since we found 2. 6% of patients harboring a hexanucleotidic expansion of C90RF72 among 114 patients with early onset dementia and CSF biomarkers indicative of AD. According to our algorithm, 18% of familial EOAD cases (age of onset (A00) before 65 years) and 14% of sporadic cases (MO before 50 years) were related to an APOE4/E4 genotype. Twenty-three percent of 168 families and 66% of 81 sporadic cases remained negative for these 3 genes and were enrolled in a pangenomic research program. Four familial and 3 sporadic cases were reported harboring copy number variants of several new genes involved in the amyloid cascade. Using next generation sequencing, 7 out of 29 unrelated familial cases harbored mutations of SORL1. Fourteen sporadic cases with combined analyses of their healthy parents allowed us to discover de novo mutations in genes related to amyloid or Tau-protein. Functional tests and large case-control studies are in progress in order to propose these genes to molecular diagnosis
Alleaume-Butaux, Aurélie. „Des maladies à prions à la maladie d'Alzheimer : vers l'identification de mécanismes communs de neurodégénérescence“. Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCB100.
Der volle Inhalt der QuellePas de résumé en anglais
Song, Pu Jiao. „Apport de l'imagerie moléculaire de la neurodégénérescence : des maladies à prion à la maladie d'Alzheimer“. Tours, 2008. http://www.theses.fr/2008TOUR3317.
Der volle Inhalt der QuelleBücher zum Thema "Maladies d'Alzheimer"
Catherine, Solano, Hrsg. Prévenir: Cancers, Alzheimer, infarctus, et vivre en forme plus longtemps. Paris: Librarie générale française, 2007.
Den vollen Inhalt der Quelle findenPloton, Louis. Maladie d'Alzheimer. 3. Aufl. Lyon: Chronique sociale, 2004.
Den vollen Inhalt der Quelle findenPierre, Thomas, Hrsg. Maladie d'Alzheimer. 2. Aufl. Paris: Masson, 1997.
Den vollen Inhalt der Quelle findenLa maladie d'Alzheimer. Paris: Jacob, 2004.
Den vollen Inhalt der Quelle findenTouchon, Jacques. La maladie d'Alzheimer. 3. Aufl. Paris: Masson, 2002.
Den vollen Inhalt der Quelle findenBernard, Michel, und Guard Olivier 1946-, Hrsg. La Maladie d'Alzheimer. Paris: MEDSI/McGraw-Hill, 1989.
Den vollen Inhalt der Quelle findenDerouesné, Christian. La maladie d'alzheimer. Paris: L'Esprit du temps, 1994.
Den vollen Inhalt der Quelle findenRousseau, Thierry. Communication et maladie d'alzheimer. Isbergues: Ortho-Edition, 1995.
Den vollen Inhalt der Quelle findenGzil, Fabrice. La maladie d'Alzheimer: Problèmes philosophiques. Paris: Presses universitaires de France, 2009.
Den vollen Inhalt der Quelle findenGzil, Fabrice. La maladie d'Alzheimer: Problèmes philosophiques. Paris: Presses universitaires de France, 2009.
Den vollen Inhalt der Quelle findenBuchteile zum Thema "Maladies d'Alzheimer"
Bosch, José Luis C. „Similitudes et différences de l'environnement d'aide d'une « nouvelle » maladie par rapport aux autres maladies“. In Exclusion, maladie d'Alzheimer et troubles apparentés : le vécu des aidants, 231–67. Érès, 2007. http://dx.doi.org/10.3917/eres.pitau.2007.02.0231.
Der volle Inhalt der QuellePariel, S., C. Kulibanov, Y. Magar und J. Belmin. „Éducation thérapeutique des aidants familiaux de patients atteints de maladie d'Alzheimer ou de maladies apparentées“. In Éducation thérapeutique, 213–22. Elsevier, 2009. http://dx.doi.org/10.1016/b978-2-294-70467-3.00025-7.
Der volle Inhalt der QuelleRoche, Yvon. „Maladie d'Alzheimer“. In Risques médicaux au cabinet dentaire en pratique quotidienne, 589–98. Elsevier, 2010. http://dx.doi.org/10.1016/b978-2-294-70866-4.00038-9.
Der volle Inhalt der QuelleHausser-Hauw, Chantal. „Maladie d'Alzheimer“. In Manuel d'EEG de l'adulte. Veille et sommeil, 145–47. Elsevier, 2007. http://dx.doi.org/10.1016/b978-2-294-07145-4.50025-8.
Der volle Inhalt der QuelleCollette, Fabienne, Dorothée Feyers und Christine Bastin. „La Maladie D'alzheimer“. In Neuropsychologie du vieillissement normal et pathologique, 105–22. Elsevier, 2008. http://dx.doi.org/10.1016/b978-2-294-70165-8.50007-8.
Der volle Inhalt der QuelleBelon, Jean-Paul. „La maladie d'Alzheimer“. In Conseils à l'officine, 265–70. Elsevier, 2009. http://dx.doi.org/10.1016/b978-2-294-70893-0.00039-x.
Der volle Inhalt der QuelleHallouët, Pascal. „Maladie d'Alzheimer (MA)“. In Mémo-guide infirmier, 261–68. Elsevier, 2010. http://dx.doi.org/10.1016/b978-2-294-71154-1.50041-x.
Der volle Inhalt der QuelleHallouët, Pascal. „Maladie d'Alzheimer (MA)“. In Méga Mémo IFSI, 1187–94. Elsevier, 2016. http://dx.doi.org/10.1016/b978-2-294-74924-7.50175-5.
Der volle Inhalt der QuelleCaire, J. M., und M. Dulaurens. „Neurosystémique et maladie d'Alzheimer“. In Handicap et Famille, 106–16. Elsevier, 2011. http://dx.doi.org/10.1016/b978-2-294-71414-6.00010-3.
Der volle Inhalt der Quelle„Bibliographie“. In Soigner la maladie d'Alzheimer, 171–73. Dunod, 2012. http://dx.doi.org/10.3917/dunod.chara.2012.01.0171.
Der volle Inhalt der Quelle